Inflammatory Bowel Disease (IBD) is an umbrella term used to describe disorders that involve chronic inflammation of the digestive tract. IBD is generally attributed to an inappropriate immunologic response to otherwise commensal flora in a genetically susceptible host. Symptoms of IBD most commonly include fever, vomiting, diarrhea, bloody stool, abdominal pain and weight loss. Types of IBD include ulcerative colitis and Crohn's disease.
Ulcerative colitis causes long-lasting inflammation and sores (ulcers) in the innermost lining of the large intestine (colon) and rectum. UC is usually characterized by inflammation of the colon and the rectum.
Crohn's disease is characterized by inflammation of the lining of the digestive tract, which often spreads deep into affected tissues. CD commonly manifests as inflammation of the small intestine, but can affect other parts of the body as well.
UC and CD are commonly regarded as autoimmune diseases, with evidence suggesting they are the result of misdirected immune response. The etiology of IBD appears to involve complex interactions of genetic predisposition, environmental factors, disruption of the intestinal microbiome and an overly aggressive immune response. In addition, evidence linking the ability of intestinal epithelial cells to modify the mucosal immune response, may suggest an invasive bacterial pathway. Imbalance in intestinal microbiota of gut friendly bacteria destroyed by antibiotics as well as opportunistic pathogens are implicating factors as well. Specifically, patients with IBD have been reported to have an abnormal gut microbiota. Whether this altered flora is the cause or the result of chronic inflammation remains unclear.
In this context, animal models have been established to provide a uniquely accurate and tractable model for studying the gut microbiota, including the molecular and cellular mechanisms driving chronic intestinal inflammation (Panwala et al., 1998; Shah et al., 1998; Pizarro et al., 2003; Sartor, 2006; Wirtz et al., 2007). The models of inflammatory bowel disease facilitate a mechanistic evaluation of the contribution of the gut microbiota to the initiation and perpetuation of chronic intestinal inflammation, as occurs in human IBD (Sartor, 2006).
There are numerous emerging therapeutic strategies, which may be useful in the alleviation of chronic intestinal inflammation, including dietary supply of non-digestible saccharides such as resistant starch (RS), inulins, fructo-oligosaccharides among others, which are carbohydrate food ingredients designated as prebiotics (Cummings and Englyst, 1987; Cummings et al., 1997; Higgins and Brown, 2013). RS, also known as Digestion Resistant Starch, is defined as the sum of starch and starch digestion products that are not digested in the small intestine but instead reach the large intestine as a fermentable fiber substrate. Resistant starch represents a diverse range of indigestible starch-based dietary carbohydrates that are not digested and absorbed in the upper digestive tract and, so, pass into the large bowel, where they undergo microbial fermentation (Asp, 1987; Topping and Clifton, 2001; Higgins and Brown, 2013). Resistant starch has been investigated in the past for its effects on bowel health (pH, epithelial thickness, and apoptosis of colorectal cancer cells), reduction in postprandial glycemia; increased insulin sensitivity; and effects on the gut microbiome (Higgins and Brown, 2013).
It is important to note however that all resistant starch is not equal. Specifically, there is exceptional diversity encountered among RS varieties. Specifically, RS varieties originating from different plant sources and/or manufactured with alternative processing technologies will possess unique physiochemical properties.
For example, a comparison of the structural properties of high amylose corn starch and potato starch (Leszczynski, 2004. Pol. J. Food Nutr. Sci 13/54: 37-50) teaches that the starch granule surface features are determined by the botanical origin of starch and, along with an increasing size of granules, they affect the specific surface area of starch. The specific surface area is diversified depending on the type of starch and ranges from e.g. 0.243 m2/g in the case of potato starch granules with type B crystallinity to 0.687 m2/g in the case of type A maize starch granules . . . . The specific surface area of starch granules and pore volume are correlated with gelatinization temperature and the viscosity of pastes obtained. The specific surface area of starch granules, as well as the number and size of pores, are also linked with the ability of starch to adsorb different substances, including protein compounds and enzymes.
The microbial complex in the colon, comprising apparently 1014 microbes of several hundred species, represents a large ecosystem, which in the right composition has a beneficial effect on the host. In this regard, the intestinal microbiota, with their immunological potency, may play an essential role in intestinal barrier resistance to ulcerative colitis (UC) (Butzner et al., 1996), and could be important in promoting large bowel health and preventing IBD among other gut ailments (Topping and Clifton, 2001). Studies utilizing mouse models of colitis have demonstrated a potential role of RS in IBD by partially preventing or ameliorating clinical disease or disease severity and prevention of inflammatory lesions (Bassaganya-Riera et al., 2011; Le Leu et al., 2013). This study therefore seeks to investigate resistant starch (MSPrebiotic®) as a potential preventive and or therapeutic tool for ulcerative colitis in a pig model of experimental colitis.